PULMONARY EMBOLISM “THE GREAT MASQUERADER” Dr. Prakash Mohanasundaram EMERGENCY PHYSICIAN

DEFINITION Pulmonary embolism (PE) is a blockage of the pulmonary artery or one of its branches, usually occuring when a venous thrombus becomes dislodged from its site of formation and embolizes to the arterial blood supply of one of the lungs.

Triad: Hypercoagulability Stasis to flow Vessel injury

RISK FACTORS HYPERCOAGULABILITY Malignancy Pregnancy Postpartum status(<4 wks) Estrogen Antiphospholipid antibodies Genetic mutations Factor V Leiden mutation Prothrombin gene mutation Factor VIII mutations Protein C deficiency Protein S deficiency VENOUS STASIS Bed rest >48 hrs Cast or external fixator Recent hospitalisation Long distance automobile or air travel VESSEL INJURY Recent surgery requiring endotracheal intubation Recent trauma requiring hospitalisation

PATHOPHYSIOLOGY Embolization Physiology Right ventricular dysfunction

EMBOLIZATION Proximal leg DVT Calf vein thrombi Upper extremity thrombosis

PHYSIOLOGY Increased pulmonary vascular resistance Impaired gas exchange Alveolar hyperventilation Increased airway resistance Decreased pulmonary compliance

DEATH “RIGHT VENTRICULAR DYSFUNCTION”

Clinical Features Symptom Percent Symptoms in Patients with Angio Proven PTE Symptom Percent Dyspnea 84 Chest Pain, pleuritic 74 Anxiety 59 Cough 53 Hemoptysis 30 Sweating 27 Chest Pain, nonpleuritic 14 Syncope 13 These are the common symptoms that are associated with PE As we mentioned in the previous slide, dyspnea and chest pain are not always preset. The explanation is that with a small V/Q mismatch, the adaptive physiology of the pulmonary vasculature and bronchi produce intermittent shortness of breath. Because of this, we are easily distracted and looking for a cardiogenic cause of the dyspnea. What about pleuritic chest pain, still not a home run! In fact, up to 25% of patients ultimately diagnosed with a PE, never had any chest pain! This is what makes the diagnosis so difficult!

Clinical Features Signs with Angiographically Proven PE Sign Percent Tachypnea > 20/min 92 Rales 58 Accentuated S2 53 Tachycardia >100/min 44 Fever > 37.8 43 Diaphoresis 36 S3 or S4 gallop 34 Thrombophebitis 32 Lower extremity edema 24 Lets look a t a couple of these: Tachycardia! Myth #2 We are all taught this is a key component of the diagnosis. Right? In fact, actually not having tachycardia is more commonly seen in patients who are found to have a PE! What about fever? If a patient has a fever, it must not be a PE, right? Not true. Although not common, Among patients with PE and no other source of fever, fever was present in one study in 43 of 311 patients (14%).

Unexplained tachypnoea, tachycardia, Hypoxia –Suspect PTE 11

PRETEST PROBABILITY

DIAGNOSING MODALITIES NON IMAGING D-Dimer ELISA ABG ECG NON INVASIVE CXR Venous ultrasonography Chest CT Lung scanning MR Contrast enhanced Echocardiography INVASIVE Pulmonary angiography (GOLD STANDARD) Contrast phlebography

D-dimer Test Fibrin split product Circulating half-life of 4-6 hours Positive assay > 500 ng/ml Quantitative test have 80-85% sensitivity, and 93-100% negative predictive value False Positives: Pregnant Patients Post-partum < 1 week Malignancy Surgery within 1 week Advanced age > 80 years Sepsis Hemmorrhage CVA AMI Collagen Vascular Diseases Hepatic Impairment Well, what is it? Basically, the assay is enzyme-linked monoclonal antibody test used to identify the protein, D-Dimer. D-Dimer itself is a unique degradation product that is produced by a plasmin mediated breakdown of cross-linked fibrin Good test with respect to its negative predictive value. The drawbacks are some of the false positives that we commonly see in the ER.

ABG Hypoxemia Hypocarbia “ LACK DIAGNOSTIC UTILITY IN PE ”

ECG Most Common Findings: Acute cor pulmonale or right strain patterns Tachycardia or nonspecific ST/T-wave changes Acute cor pulmonale or right strain patterns Tall peaked T-waves in lead II (P pulmonale) Right axis deviation RBBB S1-Q3-T3 (occurs in only 20% of PE patients) Atrial fibrillation / Atrial flutter A brief mention about the classic S1-Q3-T3, its appearance on the EKG may suggest PE, but study after study has shown it has no predictive value what so ever! But you got to know it because question writers for the boards love it!

Chest X ray Westermark’s sign focal oligemia / cut off sign Hampton’s hump peripheral wedge shaped density above the diaphragm Palla’s sign enlarged right descending pulmonary artery ALMOST ALWAYS NORMAL CHEST X RAY

WESTERMARK SIGN

HAMPTON’S HUMP

PALLA’S SIGN

Venous Ultrasonography Loss of vein compressibility ½ of pts with PE have no imaging evidence of DVT

Chest CT Principal imaging test New generation multislice scanners locates thrombi in the fifth order branches Alternative diagnosis Pneumonia Emphysema Pulmonary fibrosis Pulmonary mass Aortic pathology

V/Q SCAN

NORMAL V/Q SCAN

ABNORMAL V/Q SCAN

MR contrast enhanced Results similar compared with first generation CT Also assesses right ventricular function

Echocardiography ½ pts have normal echo DD’s Risk stratification AMI Pericardial tamponade Aortic dissection PE complicated by right heart failure Risk stratification MC CONNEL’s sign – right ventricular free wall hypokinesis with normal right ventricular apical motion

Pulmonary angiography (GOLD STANDARD) Detect emboli as small as 1 to 2 mm RESERVED FOR Technically inadequate CT scans Scans performed on older machines Pts who will undergo interventions

Pulmonary Embolus Arrow indicates abrupt termination of a pulmonary artery. Www.brighamrad.Harvard.edu/cases/bwh/images. This is an image of a PTE in a human lung. The arrow shows abrupt termination of a pulmonary artery.

TREATMENT THE EMERGENCY PERSPECTIVE

DICTUM “ABC”

RISK STRATIFICATION

TREATMENT PRIMARY THERAPY Thrombolysis Embolectomy ADJUNCTIVE THERAPY Pain relief Dobutamine Caution – volume overload SECONDARY THERAPY Anticoagulation IVC filters Pulmonary thromboendarterctomy

SCENARIO 45 year male, case of OPC poisoning Being treated with mechanical ventilation Paralysed & sedated for 2 days Develops sudden tachypnoea, tachycardia, hypotension & hypoxia

WHAT IS YOUR LINE OF MANAGEMENT

THROMBOLYSIS Recombinant tPA 100 mg iv infusion over 2 hours Streptokinase 250,000 U iv over 30 mins foll by 100,000 U/hr for 24 hrs Urokinase 4,4OO U/kg iv over 10 mins foll by 4,000 U/kg/hr for 12 hrs Alteplase 15 mg iv bolus foll by 2 hr infusion of 85 mg ( discontinue heparin during infusion)

SCENARIO 45 year male, A case of glioma Underwent craniotomy & evacuation 2 days ago Bed ridden for 2 days Develops sudden tachypnoea, tachycardia, hypotension & hypoxia

WHAT IS YOUR LINE OF MANAGEMENT

EMBOLECTOMY Indicated in pts with risk of thrombolysis Surgical embolectomy Catheter embolectomy

SCENARIO 45 year male, case of OPC poisoning Being treated with mechanical ventilation Paralysed & sedated for 2 days Develops sudden tachypnoea & tachycardia BP - Normal

WHAT IS YOUR LINE OF MANAGEMENT ECHO NORMAL WHAT IS YOUR LINE OF MANAGEMENT

Heparin / LMWH / Warfarin 80 U/kg iv bolus foll by 18 U/kg/hr Enoxaparin 1 mg/kg twice daily / 1.5 mg/kg daily Tinzaparin 175 mg/kg OD Fondaparinux <50 kg receive 5 mg, 50–100 kg patients receive 7.5 mg >100 kg receive 10 mg. Warfarin – 2.5 to 10 mg Target INR – 2.0 TO 3.0

IVC Filters INDICATIONS Active bleeding that precludes anticoagulation Recurrent venous thrombosis despite intensive anticoagulation

PREVENTION OF PULMONARY THROMBOEMBOLISM

SUMMARY > 50 % pts with DVT are associated with PE > 50 % cases do not have any signs or symptoms Common presentation can be unexplained tachycardia, tachypnoea, hypoxemia or mere anxiety Diagnosis and suspicion is purely clinical Follow up with anticoagulants is must as there is a increased risk of recurrence

PREVENTION IS BETTER THAN CURE

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